This study is a multicenter, open label dose escalation Phase I trial designed to assess the safety, pharmacokinetics and preliminary biologic activity of BMS-188667 (CTLA4lg) administered as four intravenous injections on days 1,3,16, and 29 to patients age 18-50 years with stable plaque psoriasis affecting 10-49% of their total body surface area. Study subjects must have failed due to either toxicity of inefficacy one standard psoriatic therapy. BMS-188667 (CTLA4lg) represents a new class of agents that targets the blockade of the second signal in T Cell activation. Resting T cells require at least two signals for induction of cytokine gene expression and cell proliferation. BMS-188667 (CTLA4lg) is a soluble, chimeric protein consisting of the extracellular domain of human CTLA-41g and a fragment (hinge-CH2-CH3 domains) of the Fc domain of human lgGl. CTLA4g hs demonstrated activity in a variety of divergent preclinical animal models, including transplanatation and autoimmunity. Though in each of these models, CTLA4lg disrupts the engagement of the identical family of receptors/coreceptors, data suggest that there may be a hierarchy in dosage requirements across the models studied. Higher doses of CTLA4lg appear to be required, in descending order, to abrogate a secondary humoral immune response, primary humoral immune response, autoantibody formation and a cell-mediated immune response, respectively. Th1 cells, which produce interleukin-2, tumor necrosis factor B (TNFB) and gamma- interferon, thereby activating macrophages and inducing delayed-type hypersensitivity responses, may be functionally inhibited at lower concentrations of BMS-188667 (CTLA4lg). This initial clinical trial is conducted in a patient population with a T-cell mediated disease characterized by the induction of Thl type cytokines. While psoriasis is a multifactorial disease, evidence suggests that it is immune- mediated, and that inappropriate expression of IL-2 or T-cell dysregulation may be important in the pathogenesis of psoriasis. There is increasing evidence that the T-cell is pivotally involved in the pathogenesis of psoriasis. Inflammatory cells, especially activated T lymphocytes and antigen presenting cells, are present at the dermal- epidermal junction in psoriatic plaques.